| disease | Cerebral Arachnoiditis |
The disease is characterized by thickening, adhesions, and cyst formation in the arachnoid membrane due to serous inflammation, leading to compression of the brain and cranial nerves as well as impaired blood supply.
bubble_chart Diagnosis
1. Acute, subacute, or chronic onset. There may be a history of fever, infection, cranial trauma, subarachnoid hemorrhage, or intrathecal drug injection before the illness, or systemic or head infection sites such as subcutaneous nodules, paranasal sinusitis, or otomastoiditis. There may also be a history and symptoms of conditions like brain tumors or multiple sclerosis.
2. Symptoms often spontaneously remit or relapse and worsen. The latter is often related to common colds, chilling, or fatigue.
3. Neurological symptoms vary depending on the primary site of involvement. Common manifestations include:
⑴ Posterior fossa arachnoiditis
(1) Dorsal type. The lesion primarily involves the cisterna magna, occasionally extending to both cerebellar hemispheres. Due to obstruction of the fourth ventricular outlet, the main feature is increased intracranial pressure, and chronic foramen magnum herniation may cause occipital and neck pain and stiffness. A few cases exhibit balance disorders and ataxia. When the medulla oblongata is involved, true bulbar palsy occurs. The condition progresses continuously. Cerebrospinal fluid pressure is elevated, and most cases show increased protein and cell counts.
(2) Ventral type. Primarily affecting the cerebellopontine angle, it presents with cerebellopontine angle syndrome, such as vertigo, nystagmus, ipsilateral tinnitus, deafness, peripheral facial deviation, facial pain and sensory impairment, and ataxia. The course is often recurrent, with less or delayed onset of intracranial hypertension. Cerebrospinal fluid shows grade I changes in cells and protein.
Mainly characterized by headache and focal epileptic seizures, with possible grade I hemiplegia or aphasia. Cerebrospinal fluid is mostly normal, with no elevated pressure. The progression is slow, and the course is prolonged.
⑶ Optic chiasm arachnoiditis
(1) Frontal and retro-orbital pain.
(2) Visual impairment. It may be limited to one side or gradually extend from one side to the opposite side or affect both sides simultaneously.
(3) Visual field defects. These may include central scotomas, concentric peripheral visual field narrowing, or irregular hemianopia or quadrantanopia.
(4) Optic disc changes. These may include inflammation, edema, primary or secondary atrophy. A few cases show normal optic discs despite severe visual loss.
(5) When the hypothalamus is involved, pituitary dysfunction may occur, such as drowsiness, grade I diabetes insipidus, or hypogonadism. Widespread damage may also affect the olfactory and trigeminal nerves.
(6) Most cases show normal intracranial pressure, but cerebrospinal fluid examination reveals increased protein and cell counts.
4. Based on the absence of skull changes, no displacement or filling defects in various imaging studies, and no space-occupying lesions on CT, tumors in corresponding regions can be ruled out. Optic chiasm arachnoiditis must also be distinguished from optic neuritis and retrobulbar neuritis. The latter two typically present with rapid and severe visual loss, concentric visual field narrowing, and normal filling of the chiasmatic cistern on pneumoencephalography, without pituitary or hypothalamic symptoms.
5. It may be complicated by spinal arachnoiditis, leading to spinal cord symptoms.
1. See spinal arachnoiditis.
2. For optic chiasm arachnoiditis, iontophoresis of iodine through the eyeball may also be attempted.
3. Convexity arachnoiditis of the cerebral hemisphere may be treated with low-dose radiotherapy.
4. For cases difficult to distinguish from tumors, surgical exploration may be considered. For optic chiasm arachnoiditis or posterior fossa arachnoiditis with significantly increased intracranial pressure unresponsive to decompressive medications, decompressive surgery may be attempted.
